Application | Comment | Organism |
---|---|---|
medicine | water-soluble components of cigarette smoke activate the vascular NAD(P)H oxidase. NAD(P)H oxidase-derived H2O2 activates NF-kappaB, leading to proinflammatory alterations in vascular phenotype, which likely promotes development of atherosclerosis | Rattus norvegicus |
Inhibitors | Comment | Organism | Structure |
---|---|---|---|
apocynin | smoking impaires acetylcholine-induced relaxations of carotid arteries, which can be improved by the NAD(P)H oxidase inhibitor apocynin. Vascular mRNA expression of the proinflammatory cytokines IL-1, IL-6, and TNF-alpha and that of inducible nitric oxide synthase is significantly increased by both smoking and cigarette smoke extract exposure, which can be prevented by apocynin, diphenyleneiodinium, or scavenging of H2O2 | Rattus norvegicus | |
diphenyleneiodonium | vascular mRNA expression of the proinflammatory cytokines IL-1, IL-6, and TNF-alpha and that of inducible nitric oxide synthase is significantly increased by both smoking and cigarette smoke extract exposure, which can be prevented by apocynin, diphenyleneiodinium, or scavenging of H2O2 | Rattus norvegicus |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Rattus norvegicus | - |
- |
- |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
artery | smoking impaires acetylcholine-induced relaxations of carotid arteries, which can be improved by the NAD(P)H oxidase inhibitor apocynin. Both smoking and in vitro cigarette smoke extract exposure significantly increase vascular superoxide anion production | Rattus norvegicus | - |
muscle | increased superoxide anion generation is present both in endothelial and smooth muscle cells after cigarette smoke extract exposure | Rattus norvegicus | - |